The goal of the research during the past year has been: 1) to complete work on the site at which barbiturates block excitatory synaptic transmission and 2) to determine the mechanism by which barbiturates enhance the action of GABA. Further studies on the sympathetic ganglion using quantal analysis confirmed previous conclusions that the blockade in ganglionic transmission by pentobarbital is due entirely to a postsynaptic action. Thus the number of quanta released was unaltered by pentobarbital but the size of each quanta was severely depressed. The second project involved determining how barbiturates enhance the action of GABA. For these experiments, recordings with sucrose gap were made from the ventral root of the isolated hemisected frog spinal cord. Dose response curves for GABA, B-alanine and glycine were constructed. It was found that barbiturates shift the GABA dose response curve to the left, often with a slight reduction in the slope of the curve. They had no effect on the B-alanine or glycine responses. These results suggests that bartiturates increase the affinity of the GABA receptor for GABA. Experiments are currently in progress to determine if barbiturates can interact with the sites at which bicuculline and picrotoxin act and, if so, whether this interaction can be related to the apparent change in affinity that barbiturates produce in the GABA receptor.